This increase in survival is mediated by different mechanisms: inhibition of EGFR and STAT3 pathways, reduction in the infiltration of tumor-associated macrophages in the tumor microenvironment, reduction of levels of chemokines able to attract and activate lymphocytes and monocytes, such as CXCL12 and CCL2, and decreased secretion of matrix metalloproteinases, crucial for invasion and metastasis [102]. This evidence concerns the gene CCL2 and neoplasm.